More evidence links a family of insecticides to bee colony collapse

In the US and Europe, honey bees that pollinate one-third of our crops are …

For nearly six years, a mysterious condition called colony collapse disorder (CCD) has been wreaking havoc with the honey bee population in the US and Europe. The cause of CCD remains elusive, with various fingers being pointed at mites, fungi, viruses, pesticides, and even cell phone emissions. Today, a pair of studies were published in Science that suggest that sublethal exposure to a family of common pesticides called neonicotinoids might play a contributing role in the great bee die-off.

Neonicotinoids are a relatively new family of insecticides. They work by switching receptors for a neurotransmitter (nAChRs) to the on state, causing paralysis and death in insects. They work in a similar manner to nerve gases like sarin (sarin prevents the transmitter from being broken down in the synaptic junction, causing a similar hyperactivation). Neonicotinoids are less toxic to mammals than insects, and as such rapidly gained favor for use in agriculture, where they're widely used to treat seeds. The insecticide diffuses throughout the plant as it grows, appearing in the pollen and nectar, which foraging honey bees collect and bring back to their hives.

The first study, from a team of French researchers, looked at the effect on honey bees of sublethal exposure to a neonicotinoid called thiamethoxam. They hypothesized that sublethal neonicotinoid exposure affects the bees' homing ability, which indirectly contributes to hive mortality. This hypothesis was based on previous studies, which showed that sublethal doses of neonicotinoids affect behavior in bees.

To test whether they were right, they tagged honey bees with RFID chips and gave them a treat—20 µl of a sucrose solution. Unfortunately for half the bees, their sucrose solution also contained 1.34 ng of thiamethoxam, a dose much smaller than the one need to cause significant lethality in bees. RFID readers on the hive entrances tracked the bees as they returned from the field, and mortality due to homing failure was calculated as the proportion of returning treated bees to returning control bees.

Since the researchers were interested in the effect of thiamethoxam on homing ability, they released some bees in a field that the bees had been in before, and released others in sites that the bees may or may not have previously visited. Mortality was much higher in the treated bees compared to their controls, and was higher in bees released in unfamiliar sites (31.6 percent) than familiar sites (10.2 percent).

The second study was conducted by a group from the UK. They looked at the effect of imidacloprid, the most widely used neonicotinoid, on bumble bees. Seventy five bumble bee colonies were split into three groups. The control group were fed pollen and sugar water for 14 days, and then placed in a field and left to forage for six weeks. A second group were treated with a relatively low dose of imidacloprid (6 µg/kg in pollen and 0.7 µg/kg in sugar water), with the third group receiving twice as much imidacloprid.

The colonies were weighed before being placed in the field, and then weekly once in the field. (The weight of the colony provides a general measure of its health, since it includes stored honey, immature bees, etc.) Both high and low treatment group colonies gained less weight than the control colonies during the six weeks in the field, although there was no significant difference between the two imidacloprid-treated groups.

Back in the US, commercial bee keepers and environmental groups have petitioned the EPA to ban another neonicotinoid, clothianidin; France, Germany, Italy, and Slovenia have already banned or limited the use of these insecticides. The EPA considered taking action back in 2010, but declined to do so at the time, leading to accusations that the agency approved clothianidin based in part on a fraudulent study conducted by Bayer, its manufacturer.